The carrageenan model for ulcerative colitis has been simplified bacteriologically. Starting with pools of bacterial strains isolated from cecal contents of conventional guinea pigs fed carrageenan, gnotobiotic animals have been associated with two pools which have been shown to contribute to cecal ulceration when carrageenan is administered. These two pools yielded one species, B. vulgatus, which was shown to contribute to cecal ulceration in gnotobiotic animals. Cecal contents from animals with ulcerative diseases were shown to have increased concentrations of C18:2 and C18:3, increased chemotactic activity and a cytopathic effect for Vero or WI-38 cells as compared to cecal contents from healthy animals. The chemotactic activity of these cecal contents has been shown to be due, in part, to the presence of C18:2 and C18:3. Cecal mucosa organ cultures from carrageenan treated animals have been shown to have higher levels of PGE2 and TxB2 when compared to normal animals. Preliminary data suggests that additions of PGE2 to normal cecal mucosa organ culture results in increased concentrations of LCFA in the culture medium.